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Renal > Objectives 2 > Flashcards

Objectives 2 Flashcards

1
Q

• When considering daily turnover of, for example, water and sodium, what does the amount excreted represent?

A

Amount excreted= amount filtered (+ amount secreted) – amount reabsorbed

o The amount excreted is the sum of solute collected in the tubule through glomerular filtration and tubular secretion minus the solute returned to the capillary though tubular reabsorption

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2
Q

• Recognize that in many cases, the percent of the filtered load that is reabsorbed can be adjusted in order to maintain homeostasis. Are there exceptions to this (in the table provided)?

A

.

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3
Q

• What is the difference between transcellular and paracellular routes of trans-epithelial transport?

A

.Transcellular-through the cell across the luminal and basolateral membrane. Most renal tubular transport occurs via the transcellular route.
o Paracellular- between cells, across tight junctions by simple diffusion

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4
Q

• What are the major types of trans-membrane transport systems?

A

.o Channel mediated diffusion-passive requires electrochemical gradient (ex. ion channel)
o Carrier mediated diffusion-uniport, symport, and anitport (ex. protein channels)
o Carrier mediated active transport-requires ATP to transport solutes against the electrochemical gradient

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5
Q

• What is meant by active transport?

A

.o Active transport is the movement of a substance against its concentration gradient
o If the process uses chemical energy, such as ATP, it is termed primary active transport.
o Secondary active transport involves the use of an electrochemical gradient.
o Active transport uses energy, unlike passive transport, which does not use any type of energy.

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6
Q

• What is the rate-limiting step in the reabsorption of sodium (and many other solutes)?

A

.Na+-K+-ATPase

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7
Q

• How do the transport systems for sodium across the luminal membrane of proximal and collecting tubule cells differ?

A

.o Collecting tubule
 Na+ enters the cell via luminal membrane Na+ selective ion channels
 Na+ exits the cell via Na+-K+-ATPase powered membrane pump
o Proximal tubule
 Na+ enters the cell via Na+-glucose symporter
 Na+ exits the cell via Na+-K+-ATPase powered membrane pump (see images in objectives)

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8
Q

• How is glucose reabsorbed in the proximal tubule?

A

Absolute dependence on Na+-K+-ATPase located on the basolateral membrane ii. “Downhill” flux of Na+ across luminal membrane into the cell …. facilitates “uphill” movement of glucose iii. ATPase transports Na+ across the basolateral membrane iv. Glucose uniporter transports glucose out of the cell across the basolateral membrane

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9
Q

• In absolute terms, what is the reabsorptive capacity of the proximal tubule?

A

.o Approximately two thirds of the glomerular filtrate is reabsorbed in the proximal tubule
o 180L of water is filtered per day
o 120L reabsorbed at the proximal tubule per day

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10
Q

• What is one of the principal techniques used to assess tubule function? What are some of the limitations of this technique?

A

.In vivo micropuncture
.Micropuncture by pipette is not possible due to depth of structure
 Collecting tubule
 Juxtamedullary nephron

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11
Q

• What are the some of the differences in transport capacity of the early and late proximal tubule?

A

.Solutes that are absorbed early; glucose, amino acids, HCO3-
o Cl- is reabsorbed primarily passively in the late proximal tubule
o Water is absorbed at both early and late proximal tubule

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12
Q

• What is “isosmotic” fluid reabsorption in the proximal tubule?

A

.Isosmotic fluid reabsorption is the filtration of water and solute at the lumen of the proximal tubule
o The tubular fluid and interstitial fluid both maintain approximately 300 mOsm/kg making them isosmotic

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13
Q

• How do we conceptually explain water reabsorption if tubular fluid and interstitial fluid osmolality are equal?

A

.The process of absorption occurs as a two-step process resulting in an isosmotic equilibrium between the tubule and interstitial fluid
o Solute transport creates a small trans-epithelial osmotic gradient tubular fluid is slightly hypotonic compared to interstitial fluid
o Water moves from lumen to interstitium down this osmotic gradient

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14
Q

• What are the two phases of proximal tubule fluid reabsorption?

A

.o Complete reabsorption in the proximal tubule is a two phase process
 Movement of water and solutes from the lumen to the interstitium
 Movement from the interstitium to the peritubular capillaries

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15
Q

• How can Starling forces promote fluid uptake into the peritubular capillaries?

A

.o Peritubular capillary uptake is promoted by
 Low peritubular capillary pressure, downstream of afferent and efferent renal arteriole resistance
 High peritubular capillary oncotic pressure created by water filtration and subsequent increase in plasma protein concentration

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16
Q

• What happens to the fluid if it is not taken up into the capillaries?

A

.o Excreted in urine

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17
Q

• What is meant by the concept of glomerulotubular (GT) balance?

A

.o The proximal tubule reabsorbes a constant percentage, approximately 67%, of the total filtered load this is called glomerulotubular (GT) balance
o GT balance helps maintain a relatively constant delivery of fluid to the distal nephron

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18
Q

• How can a change in efferent arteriolar resistance affect proximal tubule fluid reabsorption?

A

.o An increase in efferent arteriole resistance
o Increases glomerular capillary pressure
o Increases glomerular filtration rate (GFR)
o Proximal tubule reabsorption also increases due to
 Increased resistance resulting in a decrease in peritubular capillary pressure
 Increased resistance resulting in deceased renal blood flow (RBF) and increased filtration fraction causing an increased oncotic pressure in the peritubular capillary

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19
Q

• Describe the fundamental principles of in vivo micropuncture.

A

.

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20
Q

• What are the advantages and limitations of this technique?

A

.

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21
Q

• Describe the fundamental principles of in vitro microperfusion and identify the advantages and limitations of this technique.

A

.

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22
Q

• What is the importance of tubular secretion?

A

.The proximal tubule is the primary site of secretion for organic anions and cations
o Secretion is essential for substance which must be excreted by are poorly filtered because of
 Molecular size
 Charge
 Plasma protein binding

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23
Q

• Identify the multiple transport proteins involved in the secretion of organic anions and cations.

A

.

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24
Q

• What is the rate-limiting step in tubular secretion?

A

.o Na+-K+- ATPase

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25
Q

• How can manipulations of the secretory system affect the clearance of some drugs?

A

.Organic anion and organic cation transporters are relatively non-selective
 Blocking of transporters with inert substances to increase drug uptake is a clinical benefit of this non-selectivity
 Furosemide and bumetanide are diuretics that depend completely on tubular secretion to be effective

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26
Q

• Name some important drugs that are dependent on tubular secretion to elicit their effects?

A

 Furosemide and bumetanide are diuretics that depend completely on tubular secretion to be effective

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27
Q

• Does secretion occur at nephron sites other than the proximal tubule?

A

.

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28
Q

• How do we calculate the amount (of glucose for example) filtered, amount excreted, amount reabsorbed?

A

.Amount filtered = GFR X plasma glucose concentration (PGL) o Amount excreated = Volume X urine glucose concentration (UGL) o Amount absorbed = amount filtered – amount excreated

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29
Q

• How do we experimentally illustrate the transport maximum concept?

A

.o Using the renal handling of glucose

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30
Q

• What is meant by the terms “threshold” and “splay”?

A

.Threshold- represents the plasma concentration of glucose at which transport maximum ™ is exceeded
o Splay- represents the slight variance in transport maximum (Tm) between individual nephrons

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31
Q

• What is the relationship between GFR and plasma threshold?

A

.

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32
Q

• Why is glucose excreted in the urine in uncontrolled diabetes mellitus?

A

.Diabetes mellitus is characterized by glucose in the urine
o This is not a compensatory response of the kidney to try and lower plasma glucose concentration
o Since plasma glucose is so high the filtered load of glucose (GFR x plasma glucose concentration) exceeds tubular transport maximum
o Excess glucose cannot be reabsorbed past this point and excess spills over into the urine

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33
Q

• What are the unique renal handling characteristics of substances such as inulin and creatinine that enable them to be used to measure glomerular filtration rate?

A

.They are not reabsorbed or secreted by the nephron

o They are not metabolized or produced by the kidney

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34
Q

• What is the clearance formula? What do we mean by “clearance”?

A

.For a substance like inulin or creatinine the amount filtered is equal to the amount excreted in the urine o The clearance of inulin or creatinine equals the volume of plasma completely cleared of that solute per unit time (volume/time) equation is Cx = V x Ux/Px
o The clearance of inulin or creatinine is equal to GFR

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35
Q

• Will the calculated GFR be the same if inulin and creatinine are used simultaneously?

A

.Using inulin or creatinine when testing GFR will yield slightly different results. The same inert substance should be used with each test to ensure consistent results
o Using inulin or creatinine in addition to another solute can give a measurement of how that solute is cleared by the kidney through comparison with inulin or creatinine

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36
Q

• What is unique about the renal handling of substances such as PAH that enable them to be used to measure renal plasma flow?

A

.At low concentrations all PAH delivered to the kidney is either filtered or secreted
 PAH will not be present in the renal vein
 The amount of PAH in the renal artery will equal the amount in the urine

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37
Q

• Is the same fundamental clearance formula used to measure renal plasma flow and glomerular filtration rate?

A

.RPF = UPAH x V (volume/time)/PPAH

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38
Q

• How do we calculate renal blood flow from renal plasma flow?

A

.

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39
Q

• How does interstitial osmolality change as you progress from the cortex through the outer to inner medulla? What is responsible for these changes?

A

Interstitial osmolarity progressively increases from cortex through the outer to inner border of the medulla and is greatest at the papilla tip
o Medulla osmolality gradient is 300 > 1400 mOsm/kg from cortical junction to papillary tip
o Hypertonicity created by deposition of NaCl and urea into the medulla interstitium

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40
Q

• Are the absolute values the same for all species?

A

.No, rats have a urine concentration of 3000 mOsm/kg

o Concentration of urine is dependent on ratio of cortical to juxtamedullary nephrons

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41
Q

• Why is this unique environment so important?

A

.Interstitial hypertonicity is essential for urine concentration

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42
Q

• Are there examples of such an environment elsewhere in the body?

A

.No, the nephrons are the only cellular environment in the body that can withstand a hypertonic environment. All other cells of the body would be damaged if subjected to a hypertonic environment.

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43
Q

• How do the transport characteristics of the thin descending and ascending limbs of the loop of Henle differ?

A

.Descending limb reabsorbs water NO NaCL ABSORBPTION

o Ascending limb reabsorbs NaCL NO WATER ABSORBPTION

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44
Q

• In terms of percent of filtered load, what is the magnitude of transport in these segments?

A

.The thin descending limb is capable of reabsorbing 30-40 liters of water per day
o The thick ascending limb reabsorbs 20-25% of the NaCl filtered load

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45
Q

• What is the impact of these transport characteristics on the composition of the tubular fluid?

A

.Thin descending limb water reabsorption generates a hypertonic tubular fluid 300 to 1200 mOsm/L for long looped nephrons
o NaCl reabsorption of the thick ascending limb generates a hypotonic tubular fluid 1200 to 100 mOsm/L for long looped nephrons

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46
Q

• Will the composition of tubular fluid at the tip of short-looped nephrons be the same as that of long-looped nephrons?

A

.Composition of the tubular fluid is dependent on the length of the thin descending limb
o The longer the thin descending limb the more water is reabsorbed
 Short looped nephrons concentrate tubular fluid from 300 to 800 mOsm/L
 Long looped nephrons concentrate tubular fluid from 300 to 1200 mOsm/L

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47
Q

• Why doesn’t water reabsorption from the thin descending limb wash out the medullary interstitial osmotic gradient?

A

.o The medullary interstitial osmotic gradient is not affected because water reabsorbed from the thin descending limb is immediately transported to the vasa recta and returned to systemic circulation

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48
Q

• What is a common term for the ascending limb of the loop of Henle?; Why is it so termed?

A

.The diluting segment

o The reabsorption of NaCl results in dilution of tubular fluid

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49
Q

• What is the unique transporter on the luminal membrane of the thick ascending limb?

A

.Basolateral membrane transport is dependent on Na+-K+- ATPase
o Luminal membrane transport is dependent on Na+-K+-2Cl- co-transporter

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50
Q

• Why is the reflux of potassium back across the luminal membrane so important for transport in the thick limb?

A

.Reflux of potassium back across the luminal membrane generates a positive lumen potential that provides a driving force for paracellular transport of multiple cations (Na+, K+, Ca2+, Mg2+)
o Reflux of potassium back across the luminal membrane also ensure adequate supply of K+ for the Na+-K+-2Cl- co-transporter

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51
Q

• How are ions reabsorbed paracellularly?

A

o Na+, K+, Ca2+, Mg2+

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52
Q

• Which class of drugs can affect this transport in the thick ascending limb; how do they act?

A

.o Loop diuretic furosemide and bumetanide inhibit the Na+-K+-2Cl- co-transporter

53
Q

• Which nephron segments comprise the distal nephron?

A

.o Distal convoluted tubule and the collecting tubule consisting of cortical and papillary segments

54
Q

• What fraction of the filtered load of water and sodium remain by the time the tubular fluid arrives at the distal nephron?

A

.10% filtered load of water

o 10% filtered load of NaCl (and KCl)

55
Q

• Which two hormones regulate water and sodium reabsorption in the distal nephron?

A

.Distal nephron water reabsorption is regulated by antidiuretic hormone (ADH)
 As ADH increases water reabsorption increases and excretion decreases
o Distal nephron NaCl reabsorption is regulated by aldosterone
 As aldosterone increases NaCl reabsorption increases and excreation decreases

56
Q

• How does the composition of excreted urine differ in the states of maximal diuresis and maximal antidiuresis; how does this occur?

A

.Antidiureses
 ADH is present causing the distal collecting tubule to be permeable to water
 Osmotic gradient between the tubular fluid and interstitium promotes water reabsorption
 Urine volume is decreased and it becomes hypertonic or concentrated
o Diuresis
 ADH is absent causing the distal collecting tubule to be impermeable to water
 Some NaCl is reabsorbed further diluting the tubular fluid
 Urine volume is larger and hypotonic

57
Q

• In the absence of ADH, why does tubular fluid become even more dilute from the beginning to the end of the distal nephron?

A

.Antidiureses
 ADH is present causing the distal collecting tubule to be permeable to water
 Osmotic gradient between the tubular fluid and interstitium promotes water reabsorption
 Urine volume is decreased and it becomes hypertonic or concentrated
o Diuresis
 ADH is absent causing the distal collecting tubule to be impermeable to water
 Some NaCl is reabsorbed further diluting the tubular fluid
 Urine volume is larger and hypotonic

58
Q

• How does ADH make a collecting tubule cell permeable to water? What is the signaling system used in this process?

A

.Aquaporin’s are present in the luminal membrane of the distal collecting tubule
o ADH stimulates insertion of pre-existing aquaporin channels (AQP-2) into the luminal membrane
 ADH binds to its receptor on the basolateral membrane of the tubular cell
 cAMP is activated through a cascade then activates protein kinase A
 Protein kinase A activates aquaporin dormant within the tubular cell
 Channel containing vesicles translocate to the luminal membrane
 Aquaporin’s fuse and insert into the membrane
 Water flows through aquaporin in the luminal membrane into the tubular cell
 Water flows out of the tubular cell into the interstitium via constitutively expresses AQP-3 channels in the basolateral membrane

59
Q

• Where do the water channels (aquaporins) reside in the low ADH state?

A

.o Aquaporin’s are stored in intracellular vesicles

60
Q

• What type(s) of aquaporin are located in the luminal and basolateral membranes of collecting tubule cells?

A

.Luminal membrane-AQP-2 ascending limb does not express luminal aquaporin o Basolateral membrane- AQP-3 all nephron segments express this aquaporin

61
Q

• Are channels in both membranes inserted/retrieved under the influence of ADH?

A

.Luminal membrane aquaporin AQP-2 is activated and deactivated by ADH
o Basolateral membrane aquaporin AQP-3 is constitutively expresses

62
Q

• What is the effect of aldosterone and where does it act?

A

.

63
Q

• What is the intracellular mechanism of aldosterone action?

A

.

64
Q

• What prevents circulating glucocorticoid from affecting Na+ reabsorption?

A

.

65
Q

• How does parathyroid hormone stimulate calcium reabsorption in the distal tubule?

A

.

66
Q

• How does the onset-time for aldosterone action compare to that of ADH? Why do they differ?

A

.

67
Q

• What is countercurrent multiplication?

A

.Deposition of sodium chloride

68
Q

• Why is it essential for the deposition of NaCl in the medullary interstitium?

A

.Deposition of NaCl in the medullary interstitium would not be possible without countercurrent multiplication because only isotonic fluid containing approximately 100 mM NaCl would flow through the ascending limb into the distal tubule

69
Q

• How can countercurrent multiplication be broken down into a conceptual 3-step model?

A

.Reabsorption of NaCl by the ascending limb results in retention in the interstitium
o Reabsorption of water by the descending limb and transfer to the vasa recta
o Isotonic fluid from proximal tubule into the loop is converted to hypertonic fluid into the ascending tubule
o Repeating these three steps generates vertical interstitial osmotic gradient 325-600 mOsm

70
Q

• How do the urea transport characteristics of the subsections of the collecting tubule differ?

A

.Cortical and outer medullary collecting tubule cannot reabsorb urea. Urea concentration of the tubular fluid increases due to absorption of water that results in a hypertonic tubular fluid
 Water moves from tubular fluid to interstitium
 Urea remaining in the reduced tubular fluid volume is more concentrated
o When tubular fluid reaches the inner medullary collecting tubule urea concentration is higher than the interstitium urea is passively reabsorbed into the interstitium of the medulla down its concentration gradient

71
Q

• Why is ADH so critical for urea reabsorption; what is meant by urea recycling?

A

.ADH activates luminal aquaporin’s of the collecting tubule resulting in water reabsorption that is responsible concentration of urea in the tubular fluid creating an osmotic gradient between the tubular fluid and interstitium
o Reduction in ADH results in less water re-absorption that would cause less concentration of urea reducing the osmotic gradient between the tubular fluid and interstitium causing less urea to be reabsorbed in the inner medulla. Urea would be excreted.

—What is meant by urea recycling?
o Some of the urea in the medulla diffuses back into the tubular fluid in the thin descending and ascending limbs
o The urea that re-enters the tubule from the interstitium is processed again in the distal collecting tubule through the same process and re-deposited back into the interstitium
o This maintains inner medullary hyper tonicity allowing for urine concentration

72
Q

• If ADH levels decrease, why do the medullary interstitial levels of both urea and NaCl decrease?

A

.ADH levels decrease causing urea concentrations to decrease due to
 A reduction in urea concentration corresponding to reduction in water reabsorption
 Increase of urea excretion in the tubular fluid
 Resulting in a decrease in medullary osmolality
 Causes decreased water reabsorption in the thin descending limb
 Causes decreased NaCl reabsorption in the thin ascending limb reducing interstitial NaCl
 Decreases medullary osmolarity
o An increase in ADH levels reverses this process resulting in re-deposition of NaCl and urea which increases the medullary osmolality

73
Q

• What is meant by countercurrent exchange?

A

.Passage of solute in opposite directions between two flowing bodies
o In the kidney countercurrent exchange occurs between the interstitium and the vasa recta resulting in maintenance of the interstitium hypertonicity

74
Q

• Why does the osmolality of plasma increase in the vasa recta as it flows into the medulla?

A

.The plasma in the vasa recta is hypertonic compared to the interstitial fluid due to the concentration of NaCl and urea. This osmotic gradient causes NaCl and urea from the interstitium to flow into the plasma of the vasa recta resulting in a reduction of the medullary hypertonicity and increasing the osmolality of the plasma.

75
Q

• Why is the medullary interstitial gradient preserved?

A

.As the vasa recta turns in the medulla and travels back toward the cortex the osmolarity of the plasma exceeds that of the interstitium causing the osmotic gradient to reverse. NaCl and urea flow from the plasma of the vasa recta returning to the interstitium preserving the interstitial gradient that maintains the hypertonicity of the medulla.

76
Q

• Why is flow rate and solute content of plasma exiting the medulla higher than that entering?

A

The vasa recta’s main function is to remove all water from the interstitium that is reabsorbed by the nephron descending limb and medullary collecting tubules. This water reabsorption increases the plasma flow rate.
o The vasa recta is also responsible for removing most of the NaCl reabsorbed by the ascending limb. This increases the solute content of the vasa recta plasma as it exits the medulla.

77
Q

• Describe the challenges to cell survival of a hypertonic interstitial environment.

A

.

78
Q

• Describe the mechanisms involved in maintaining cell structure and function.

A

.

79
Q

• What is meant by the balance concept?

A

.Water input is equal to water output

80
Q

• What are the major sources of water input and water output from the body?

A

.Input- food intake, fluid intake, and metabolism
o Output- insensible losses, feces, sweat, and urine
 Urine is the best control point for adjustment of water excretion or retention
 Insensible losses are diffusion through skin or exhalation

81
Q

• What are the extremes of urine volume and osmolality in diuresis and antidiuresis?

A 
.Maximum diuresis (water excretion)
 Urine volume: 20-25 L/day
 Urine osmolality: 50-75 mOsm/kg
o Maximum antidiuresis (water conservation)
 Urine volume: 0.5 L/day
 Urine osmolality: 1200-1400 mOsm/kg
82
Q

• Why, in cases of extreme water deficit, can we not stop urine output completely to conserve water?

A

.Even in a state of dehydration maximum antidiuresis cannot decrease below 0.5 L/day because this minimum fluid volume is required to excrete metabolic wastes that are toxic to the body and must be removed.

83
Q

• What class of hormone is ADH?

A

.Peptide hormone

84
Q

• Where is it synthesized, stored and secreted?

A

.Synthesized in the neural cell bodies located in supraoptic and paraventricular nuclei of the hypothalamus.
o Transported via neural axons from the hypothalamus to the posterior pituitary. Stored in the nerve terminals of the posterior pituitary
o Secreted by the posterior pituitary

85
Q

• What are the two principal mechanisms that regulate ADH secretion?

A

.Osmoreceptors
 Most important mechanism
 pituitary
 Plasma osmolarity in excess of 300 mOsm/L triggers ADH secretion
 Increase in plasma osmolarity> secretion of ADH> increased water reabsorption in the kidney> decreases plasma osmolarity
o Volume receptors
 Decrease in blood plasma volume> secretion of ADH> increased water reabsorption in the kidney> increases plasma volume

86
Q

Which mechanism is the more sensitive?

A

Osmoreceptors are more sensitive. Less than 1% increase in osmolarity of blood plasma results in secretion of ADH by posterior
o Volume receptors require 10% change in blood volume for activation

87
Q

Do these two systems interact?

A

Yes, changes in the blood plasma volume effect the blood plasma osmolarity
 Increase in volume causes a decrease in osmolarity, set point increases
 Decrease in volume causes an increase in osmolarity, set point decreases
o Any change in volume that effects the set point will trigger ADH release through osmoreceptors

88
Q

What is the osmotic set point?

A

The osmolarity at which ADH will be secreated

89
Q

• Are large changes in plasma ADH required to elicit changes in urine volume and osmolality?

A

No, small changes in plasma ADH cause large changes in urine concentration and volume
 Increase in ADH> increases urine osmolarity> decreases urine volume

90
Q

• In a state of water deficit, will an increase in ADH and thus increased water reabsorption alone restore normal fluid volume? • How is thirst controlled?

A

No, fluid replacement is required to completely restore total body water levels to homeostasis
o Secretion of ADH decreases urine volume which only minimizes further water loss it does not correct a water deficit
o A decrease in total body water that increases extracellular osmolarity also stimulates thirst receptors

91
Q

.

A

.

92
Q

• What is SIADH; what are the possible causes; what are the potential effects?

A

.SIADH- syndrome of inappropriate ADH secretion
o Causes
 Head trauma, encephalitis, meningitis
 ADH secreting tumors (lung, pancreas)
 Drug-induced (nicotine, morphine, chemotherapeutic agents)
o Effects
 Increased ADH> increased water reabsorption> hyponatremia (dilute extracellular fluid)
 Decreased serum Na+> decreased plasma osmolarity> influx of water into cortical neurons> coma

93
Q

• What are the two principal forms of diabetes insipidus?

A

.Hypothalamic (central)
 Decreased production or release of ADH from the hypothalamus
 Lack of pituitary secretion of ADH
o Nephrogenic
 Kidney is unresponsive to ADH
 Genetic familial mutation of ADH receptor causing lack of cAMP activation resulting in no aquaporin activation
 Genetic familial mutation that

94
Q

• Can they be treated? If not, how can a subject remain in water balance?

A

.Hypothalamic can be treated with synthetic ADH nasal spray
o Nephrogenic cannot be treated. Patient must increase water intake to replace the excessive water lost due to lack of aquaporin function.

95
Q

• How can the measurement of free water clearance provide an assessment of ascending limb function?

A

.The ascending limb reabsorbs NaCl.
o Free water clearance represents the amount of distilled water that must be added to or removed from urine to create and isotonic fluid
o The free water clearance is an assessment of how effectively the thick ascending limb is reabsorbing NaCl there by creating a hypotonic tubular fluid (NaCl diffuses from tubular fluid into interstitium)
o Diseases like Addison’s and Bartter’s syndrome effect sodium reabsorption at the thick ascending limb reducing the amount of free water clearance

96
Q

• Is the standard clearance formula (GFR; RPF) used to measure free water clearance?

A

.No, the formula used for free water clearance is: CH2O = V–VxUOSM
POSM (rewrite this correctly)

97
Q

• When is free water clearance zero?

A

.When urine excreted is isotonic to interstitial fluid at 300 mOsm/L water clearance is zero

98
Q

• What alternative term is used when a hypertonic urine is excreted?

A

.Free water absorption, is the term used when hypertonic urine is excreted

99
Q

• Why is extracellular fluid volume directly related to total body sodium content (a more comprehensive description than in section 1)?

A

.Extracellular fluid volume is directly related to total body sodium content due to water flow between intracellular and extracellular compartments resulting from changes in tonicity
 Changes in fluid volume also effect ADH secretion with alters reabsorption of water
 Changes in fluid volume effect extracellular osmolarity that triggers thirst

100
Q

• What is the role of the kidneys in maintenance of a normal extracellular fluid volume?

A

.Kidneys maintain constant extracellular volume by adjusting NaCl excretion to match NaCl intake

101
Q

• What is the role of aldosterone in this system; where does it act?

A

.Na+ secretion is primarily regulated by aldosterone action

o Aldosterone acts on the cortical collecting tubule

102
Q

• What is the intracellular mechanism of aldosterone action?

A

.Extracellular NaCl decreases> aldosterone is secreated> Na+ reabsorption increases> Na+ excretion decreases
o Aldosterone is a steroid hormone that easily crosses the plasma membrane and enters the cell to bind with intracellular receptors
o Activation within the nucleus by aldosterone alters DNA transcription and protein synthesis of the cell
o The cell increases production of proteins forming more sodium channels, Na+-K+-ATPase units, and stimulates the Krebs cycle generating energy for the cell and increasing ATPase activity.

103
Q

• How does the onset-time for aldosterone action compare to that of ADH? Why do they differ?

A

.Action of aldosterone takes hours for effects to be seen in Na+ reabsorption
 time is required for DNA transcription, protein synthesis, and incorporation of new membrane channels
o ADH action takes only minutes
 ADH is a protein hormone that binds to surface membrane receptors causing activation of cAMP
 Aquaporin activation takes less time than synthesis of proteins

104
Q

• Why is the measurement of extracellular fluid sodium concentration not a reliable index of total body sodium content?

A

.When sodium concentration increases rapidly extracellular volume increases in response which returns the sodium concentration to the previous value.
o This change in extracellular fluid volume is a more reliable index of total body sodium content than the concentration of sodium.

105
Q

• What is the “effective circulating volume”? How is the status of this compartment monitored?

A

.Effective Circulating Volume (ECV) is the volume of arterial blood (vascular extracellular fluid) effectively perfusing tissue. ECV is a dynamic quantity and not a measurable, distinct compartment.

106
Q

• What is the rate-limiting step in this process?

A

.Renin release from the kidney

107
Q

• Can renin be classified as a hormone?

A

.No, renin is an enzyme

108
Q

• Where is angiotensinogen synthesized?

A

.The liver

109
Q

• Where is angiotensin I converted to angiotensin II?

A

.In the lung by converting enzyme

110
Q

• Where is aldosterone synthesized?

A

.Zona glomerulosa of the adrenal cortex

110
Q

• What are the three mechanisms that can regulate renin release?

A

.

111
Q

• In the macula densa mechanism, why isn’t GFR restored to normal by autoregulation-TG-feedback?

A

.

112
Q

• What are the three mechanisms that can regulate renin release?

A

.Where is renin synthesized?
o This enzyme is secreted by the kidney from specialized cells called granular cells of the juxtaglomerular apparatus
 What are the three mechanisms that can regulate renin release?
o A decrease in arterial blood pressure detected by baroreceptors
o A decrease in GFR measured by the macula densa of the juxtaglomerular apparatus.
o Sympathetic nervous system activity, which also controls blood pressure

114
Q

• What do we mean by “rapid-onset” effects of angiotensin II?

A

.Attempt to restore normal blood pressure
 Peripheral vasoconstriction increases peripheral resistance
 Increased afferent arteriole resistance increases peritubular capillary pressure
 Increased heart rate increases cardiac output

115
Q

• Why are these mechanisms alone not sufficient to restore normal blood pressure after for example, hemorrhage?

A

.Extracellular volume loss must be replaced for blood pressure to return to homeostasis

115
Q

• Explain the concept of aldosterone escape.

A

.

116
Q

• List the longer-term effects of angiotensin II that restore total body sodium and water to normal.

A

.Long term effects of angiotensin II decrease NaCl and water excretion in addition to increasing NaCl and water intake
 Increases proximal tubule reabsorption of water and NaCl
 Activates aldosterone increasing reabsorption of water and NaCl at the distal convoluted tubule and collecting duct
 Activates antidiuretic hormone increasing collecting duct water reabsorption
 Activates thirst increasing water intake

118
Q

• What is meant by “positive” and “negative” sodium balance?

A

.Positive sodium balance: intake > excretion

o Negative sodium balance: intake

119
Q

• What is the most direct indicator that you are in one of these states?

A

.Water retention or excretion

120
Q

• Why can the kidneys not compensate for a sudden and sustained change in sodium intake?

A

.Renal compensation for sudden changes in NaCl intake take several days
o The speed of change is due to the mechanism of aldosterone action
 Steroid hormone
 Alters DNA transcription and protein synthesis

121
Q

• Where is atrial natriuretic peptide synthesized; what stimulates its release?

A

.Synthesized by atrial myocytes

o Release stimulated by an increase in extracellular volume

122
Q

• What are the principal mechanisms of ANP action that lead to increased salt and water excretion?

A

.Secretion of ANP> increased NaCl and water excretion due to
 Vasodilation of the afferent arteriole at the glomerulus increasing glomerular filtration rate
 Inhibition of aldosterone secretion via direct action of the zona glomerulosa cells or inhibition of renin release
 Inhibition of NaCl reabsorption in proximal tubule and collecting tubule
 Antagonized ADH action via inhibition of ADH release or inhibition of ADH action on the collecting tubule

123
Q

• Is ANP an important regulator of sodium balance under “normal” circumstances?

A

.o No
o Natriuretic peptides are peptide hormones that are synthesized by the heart, brain and other organs. The release of these peptides by the heart is stimulated by atrial and ventricular distension, as well as by neuro-humoral stimuli, usually in response to heart failure.

124
Q

• What is the primary cause of Bartter’s syndrome?

A

.Mutations in the gene expressing the Na+-K+-Cl- cotransporter (ENCC2) and/or luminal K+ (ROMK) channel in the thick ascending limb

124
Q

• What is PKD?

A

.

125
Q

• Explain the physiological abnormalities that occur in this syndrome.

A

.renal salt wasting decreased NaCl reabsorption causes increased NaCl excretion
o volume depletion increased NaCl excretion causes increased H2O excretion
o hyperreninemic hyperaldosteronism
o hypercalciuria caused by a reduction in lumen positive potential
o hypokalemic metabolic alkalosis

126
Q

• Name the principal classes of diuretics; where do they act and what are their mechanism(s) of action.

A

.

128
Q

• What is edema; what are the principal causes of this problem?

A

.The accumulation of excess fluid in the interstitial space.
Altered balance of starling forces across the systemic capillaries resulting in an influx of fluid into the interstitial space

129
Q

• How do the kidneys, by functioning perfectly appropriately, potentiate the edematous state?

A

.Edema causes a decrease in extracellular volume which activates aldosterone though volume receptors
o Aldosterone activation results in retention of NaCl and water that decreases the plasma protein concentration
o The osmotic gradient created by hypotonic plasma results in an even greater increase in the interstitial fluid volume which exacerbates edema

Renal (3 decks)

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